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dc.contributor.authorTsai, Min-Shanen_US
dc.contributor.authorHuang, Chien-Huaen_US
dc.contributor.authorTsai, Shang-Hoen_US
dc.contributor.authorTsai, Chia-Yingen_US
dc.contributor.authorChen, Huei-Wenen_US
dc.contributor.authorCheng, Hsaio-Juen_US
dc.contributor.authorHsu, Chiung-Yuanen_US
dc.contributor.authorWang, Tzung-Dauen_US
dc.contributor.authorChang, Wei-Tienen_US
dc.contributor.authorChen, Wen-Joneen_US
dc.date.accessioned2014-12-08T15:28:14Z-
dc.date.available2014-12-08T15:28:14Z-
dc.date.issued2012-10-01en_US
dc.identifier.issn0735-6757en_US
dc.identifier.urihttp://dx.doi.org/10.1016/j.ajem.2012.01.001en_US
dc.identifier.urihttp://hdl.handle.net/11536/20449-
dc.description.abstractIntroduction: Ventricular fibrillation (VF) and asphyxia account for most cardiac arrests but differ in cardiac arrest course, neurologic deficit, and myocardial damage. In VF resuscitation, cardiac mitochondria were known to be damaged via excess generation of reactive oxygen species. This study evaluated the difference of cardiac mitochondrial damages between VF and asphyxial cardiac arrests. Methods: In the VF + electrical shock (ES) group, VF was induced and untreated for 5 minutes, followed by 1 minute of cardiopulmonary resuscitation (CPR) and 1 ES of 5 J. Animals were killed immediately after ES. In the asphyxia group, cardiac arrest was induced by airway obstruction, and then pulselessness was maintained for 5 minutes, followed by 1 minute of CPR. The animals were killed immediately after CPR. The histology and ultrastructural changes of myocardium and complex activities and respiration of mitochondria were evaluated. The mitochondrial permeability transition pore opening was measured based on mitochondrial swelling rate. Results: The histopathologic examinations showed myocardial necrosis and mitochondrial damage in both cardiac arrests. Instead of regional damages of myocardium in the VF + ES group, the myocardial injury in the asphyxia group distributed diffusely. The asphyxia group demonstrated more severe mitochondrial damage than the VF + ES group, which had a faster mitochondrial swelling rate, more decreased cytochrome c oxidase activity, and more impaired respiration. Conclusions: Both VF and asphyxial cardiac arrests caused myocardial injuries and mitochondrial damages. Asphyxial cardiac arrest presented more diffuse myocardial injuries and more severe mitochondrial damages than VF cardiac arrest. (c) 2012 Elsevier Inc. All rights reserved.en_US
dc.language.isoen_USen_US
dc.titleThe difference in myocardial injuries and mitochondrial damages between asphyxial and ventricular fibrillation cardiac arrestsen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.ajem.2012.01.001en_US
dc.identifier.journalAMERICAN JOURNAL OF EMERGENCY MEDICINEen_US
dc.citation.volume30en_US
dc.citation.issue8en_US
dc.citation.spage1540en_US
dc.citation.epage1548en_US
dc.contributor.department電子工程學系及電子研究所zh_TW
dc.contributor.department電機工程學系zh_TW
dc.contributor.departmentDepartment of Electronics Engineering and Institute of Electronicsen_US
dc.contributor.departmentDepartment of Electrical and Computer Engineeringen_US
dc.identifier.wosnumberWOS:000309813900033-
dc.citation.woscount7-
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